Grace E. Stutzmann (Beth), Ph.D.

My research interests focus on studying the early neuronal
pathology that develops in Alzheimer's disease (AD), long before the deposition
of plaques and tangles and cognitive decline. To accomplish this, I use
transgenic mice that have been engineered to express the human gene mutations
that cause the inheritable form of AD. With these mice, I can examine within
individual neurons how the AD mutations impair neuronal functioning and
synaptic transmission across various stages of the disease process, with the
goal of finding ways to block or reverse these impairments. By the time memory
loss occurs in humans, the damage to the brain is often too extensive to
reverse. My previous studies show that specific calcium-mediated signaling
pathways are highly dysregulated in AD, and over time, may facilitate the
formation of amyloid plaques and tangles, interfere with neuronal signaling
processes that support learning and memory, and eventually kill the cell. To
achieve these goals, I use innovative techniques to study real-time activity in
living neurons, such as in vitro electrophysiology combined with 2-photon and
CCD imaging of calcium signals within cellular compartments. In addition,
extracellular recording techniques, immunohistochemistry, molecular biology and
behavioral approaches are also incorporated. I am also examining target
compounds that can impede the progression of AD pathology. The strategy is to
normalize aberrant signaling pathways that are present prior to the formation
of late stage markers of the disease.